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  • Author: Seiichiro Saito x
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Naoto Yoneda, Minoru Irahara, Seiichiro Saito, Hirokazu Uemura and Toshihiro Aono

Yoneda N, Irahara M, Saito S, Uemura H, Aono T. Usefulness of recombinant human prolactin for treatment of poor puerperal lactation in a rat model. Eur J Endocrinol 1995;133:613–7. ISSN 0804–4643

Recombinant human prolactin (r-hPRL) was produced by a line of murine C127 cells transfected with human PRL gene. To assess the biological efficacy of r-hPRL in vivo, we studied its influence on milk secretion using a rat model in which lactation was reduced by bromocriptine treatment. Puerperal rats were injected daily for 9 days after delivery with bromocriptine or bromocriptine plus r-hPRL, and lactational performance was assessed by weighing the pups. The concentrations of rat and human PRL in rat serum were measured by specific radioimmunoassays and the mammary glands were examined on postpartum day 10. Daily injection of bromocriptine (0.1 mg/rat) significantly reduced the endogenous level of rat PRL and impaired the weight gain of the pups. Administration of r-hPRL increased the serum level of human PRL. Daily injections of r-hPRL (50 μg/rat, twice a day) restored lactational performance and significantly increased the weight of the pups. The detrimental effect of bromocriptine on the mammary glands, assessed by both weight and histological appearance, was reversed by administration of r-hPRL. These results demonstrate that r-hPRL is biologically active in vivo and replacement therapy of r-hPRL is effective in improving the lactational performance in bromocriptine-treated rats, and also that r-hPRL may be useful for the treatment of women with poor lactation.

Naoto Yoneda, Department of Obstetrics and Gynecology, School of Medicine, The University of Tokushima, 3-18-15 Kuramoto, Tokushima 770, Japan

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Seiichiro Saito, Keiji Shitsukawa, Minoru Irahara, Toshiya Matsuzaki and Toshihiro Aono

The effects of 2-buten-4-olide (2-B40), an endogenous feeding suppressant, on the secretion of luteinizing hormone (LH) were studied in ovariectomized rats. Intraperitoneal (ip) administration of 2-B40: adult female ovariectomized Wistar rats were given daily ip injections of solution containing 2-B40 at 0, 50 or 100 mg/kg body wt for 14 days. This ip treatment with 2-B40 significantly decreased the mean LH concentration and pulse frequency of LH. Intravenous (iv) administration of 2-B40: a solution of 2-B40 (50 or 100 mg/kg body wt) was slowly injected through an intra-atrium catheter and blood samples were taken every 6 min for 2 h. This iv treatment significantly suppressed the LH pulse frequency but had no significant effect on the LH amplitude or mean LH. Injection of 2-B40 into the third cerebroventricle: the injection of 2-B40 into the third cerebroventricle of freely moving rats decreased the mean LH concentration and the frequency and amplitude of LH pulses. Third cerebroventricle injection of a corticotropin-releasing factor (CRF) receptor antagonist before third cerebroventricle injection of 2-B40: the specific CRF receptor antagonist α-helical-CRF (9–41) was injected into the third cerebroventricle of ovariectomized rats before injection of 2-B40. Administration of 2-B40 into the third cerebroventricle significantly decreased the mean LH, concentration and pulse frequency. Third cerebroventricle injection of the CRF antagonist at 50 μg/rat and then 2-B40 also resulted in significant suppression of the mean LH concentration and pulse frequency. These findings suggest that 2-B40 may suppress gonadotropin-releasing hormone secretion in ovariectomized rats and that its effect in decreasing LH pulses may not be caused through the CRF pathway.

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Hiroshi Ikawa, Minoru Irahara, Toshiya Matsuzaki, Seiichiro Saito, Toshiaki Sano and Toshihiro Aono

Prolactin (PRL) secretion in streptozotocin-induced diabetic rats postpartum was examined to elucidate the reason for the reduced milk secretion of diabetic mothers. Pregnant Wistar rats were given citrate buffer (control group) or streptozotocin only (DM group) or with insulin (insulin group). Growth of pups was significantly lower in the DM group than in the control group, but similar in the insulin and control groups. Suckling-induced PRL secretion was significantly lower in the DM group than in the control group, and intermediate in the insulin group. TRH-induced PRL secretion was significantly lower in the DM group than in the control group, but the same in the insulin and control groups. Histologically, the mammary glands in the DM group were relatively less developed than those in the control group. The results suggest that reduced milk secretion in diabetic mothers is due to impaired induction by suckling of PRL secretion from the anterior pituitary as well as poor development of the mammary gland.